More recently, by reducing the oxidative-stress-induced production of ECM genes and LC cell proliferation trough a signalling pathway mechanism involving nuclear factor of activated T-cells (NFATc3), we found that the voltage non-dependent, stretch-activated cation channels, transient receptor potential canonical TRPC1 and TRPC6, are highly expressed in glaucoma LC cells and are also involved in the aberrantly elevated intracellular [Ca2+]i levels found in glaucoma LC cells [26]. Here, TRPC1 is linked to glaucoma.